Clinical, electromyographic, electrophysiological and pharmacological evidence strongly suggests that an abnormality of the sarcolemma accounts for the myotonia of myotonic muscular dystrophy and certain other myotonic syndromes. Sarcolemma from these patients will be compared with sarcolemma of normal humans. Special attention will be paid to Mg ions, (Na plus K ions) and Ca ions ATPase of the sarcolemma and to the lipid composition of sarcolemma from normal and diseased muscle. Similar studies of sarcolemma from patients with other dystrophies, myopathies and neuromuscular diseases will be done to assess the specificity of changes detected in sarcolemma from myotonic patients. Study of ATPases and lipid composition from fast-twitch and slow-twitch muscles will be undertaken because of the known predilection for slow-twitch fiber atrophy in myotonic dystrophy. Diazacholesterol- induced myotonia in the rat and the heritable myotonia of Tennessee goats will be studied as models of human myotonia. Our studies correlating biochemistry, physiology and histochemistry of various fiber types will be expanded to yield the blood flow characteristics of the three fiber types. Using this information we will further explore the mechanisms by which various types of skeletal muscle adapt to exercise, with special reference to alterations in blood flow and their relationship to endurance and oxidative capacity.